On the ultimate free lunch:Engineering without an engineer.

Mimicking Seahorse Tails Could Lead to Better Robots

Casey Luskin July 7, 2015 11:33 AM 

 

An article at Live Science, "Seahorse's Amazing Tail Could Inspire Better Robots," describes a paper in Science on the unique shape of the tail of the seahorse. Researchers propose that its shape could provide improved architecture for robotic appendages:

Seahorses are of special interest to robot researchers because of their unusual skeletal structure, which scientists say could help them design bots that are hardy and strong yet also flexible enough to carry out tasks in real-world settings. "Human engineers tend to build things that are stiff so they can be controlled easily," study co-author Ross Hatton, an assistant professor in the College of Engineering at Oregon State University, said in a statement. "But nature makes things just strong enough not to break, and then flexible enough to do a wide range of tasks. That's why we can learn a lot from animals that will inspire the next generations of robotics."

Seahorses are true fish, classified as ray finned fishes, a subclass of the bony fishes. But they have a unique skeletal architecture in their tails, which in cross-section are square rather than round:

In particular, seahorses have square (rather than round) bony plates that surround the "backbone" of their tails. These odd features help the fishes bend, twist and get a stronger grip on their surroundings. But, the square structures also make them more resistant to being crushed by predators, the researchers said.

A summary article in Science explains the mechanical advantages of this unique and robust design:

Most animals and plants approximate a cylinder in shape, and where junctions occur (as with branches of trees or limbs on animals), those corners are "faired," meaning smoothly curved so that one surface grades into the next (1). When living organisms deviate from the norm, there's usually a good biomechanical reason: a clue to some specific problem that needs to be solved. Among their suite of unusual characteristics, seahorses possess a true oddity: a prehensile tail with a square, rather than round or elliptical, crosssectional shape. On page 46 of this issue, Porter et al. (2) report that there are distinct mechanical advantages to being square. Using threedimensional (3D) printing to construct physical models, the team demonstrates that the multiplated anatomy of the square seahorse tail shows greater resistance to mechanical deformation than a similar model that has a round cross section. ... Porter et al. suggest that a square tail provides superior resistance against compressive injury (i.e., a bite from a predator)

The technical paper in Science elaborates:

[T]he square prism is more resilient when crushed and provides a mechanism for preserving articulatory organization upon extensive bending and twisting, as compared with its cylindrical counterpart. Thus, the square architecture is better than the circular one in the context of two integrated functions: grasping ability and crushing resistance.

So why is this shape more robust than a cylindrical or circular one? A square ring made of multiple plates on each side can retain its shape while being compressed under stress, and then return to its normal shape because the plates can slide past one-another. A circular ring, however, cannot do so without losing its shape and becoming permanently deformed. As the paper explains, "a square ring changes size but not shape when biaxially compressed because of the ability of the corner plates to slide over one another," whereas "a round ring cannot retain its shape when biaxially compressed, because the plates interfere with one another." This is a keen design that allows the tail to both bend and accommodate stresses without losing its shape.

The paper explains how the design could be put to use by human engineers:

Beyond their intended practical applications, engineering designs are  convenient means to answer elusive biological questions when live animal data are unavailable (for example, seahorses do not have cylindrical tails). Understanding the role of mechanics in these prototypes may help engineers to develop future seahorse-inspired technologies that mimic the prehensile and armored functions of the natural appendage for a variety of applications in robotics, defense systems, or biomedicine.

Here's how the authors conclude their paper after studying the engineering design of the seahorses tail:

The highly articulated bony plates that surround the central vertebral axis of a seahorse tail actively facilitate bending and twisting as well as resist vertebral fracture from impact and crushing. To explore why the bony plates are arranged into cross-sectional squares rather than circles, we analyzed themechanics of 3D-printed models that mimic the natural (square prism) and hypothetical (cylindrical) architectures of a seahorse tail skeleton. Physical manipulation of the two prototypes revealed that the square architecture possesses several mechanical advantages over its circular counterpart in bending, twisting, and resistance to crushing. The enhanced performance realized in the square architecture provides insight into the way in which seahorses may benefit from having prehensile tails composed of armored plates organized into square prisms, rather than cylinders. This study demonstrates that engineering designs are convenient means to answer elusive biological questions when biological data are nonexistent or difficult to obtain.

These papers are peppered with claims that the square shape "evolved" because of the mechanical advantages it provided. But simply identifying the advantages a system provides -- and asserting they evolved -- does not constitute a Darwinian evolutionary explanation. It seems that the best way to study the operation of these structures is to treat them as engineered systems that are designed with some kind of a purpose. Scientists can pay lip service to Darwinian evolution, but it isn't helping them understand nature.

 

irreducible complexity revisited.

In Time for Michael Behe's Book Anniversary, Here's a Real Mousetrap in the Cell
Evolution News & Views

Later this year will mark the twentieth anniversary of Michael Behe's  Darwin's Black Box, a book that gave profound impetus to the burgeoning intelligent design movement. With that in mind, we want to highlight examples of discoveries that vindicate Behe's arguments in the book. Today, here is one buried in a scientific paper that might have been missed. It's especially delightful because it brings to life an analogy Behe made famous: the mousetrap as an example of irreducible complexity.Dr. Behe defined irreducible complexity as "a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning" (p. 39). A few pages later, he explained how the "humble mousetrap" meets the requirements of an irreducibly complex system: it has a function (catching mice), and all five parts (base, spring, hammer, catch and holding bar) are necessary for that function.Behe had said that "An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution." In subsequent chapters, he provided many examples in nature, from molecular machines in the cell like the cilium and flagellum, to whole-body systems like the blood clotting cascade.

Now a new example: a molecular machine that works like a mousetrap. How cool is that? No kidding, here's how the authors of a paper in the Proceedings of the National Academy of Sciences describe serpin antithrombin III (for short, ATIII):

Here the cellular folding pathway of the serpin antithrombin III (ATIII), which inhibits proteases involved in the coagulation cascade, was determined. ATIII uses a large conformational movement in a mousetrap-like mechanism to bind and distort its target protease, resulting in protease inhibition. This work establishes that folding to an active, cocked state requires early stabilization of the C-terminal region, which is the last sequence translated, explaining how the serpin or mousetrap is set. [Emphasis added.]
Oh, this is good. Here we find a mousetrap, a molecular machine, and the blood clotting cascade brought together in a single irreducibly complex protein. And proteins, we all know, are coded by complex specified information -- another hallmark of intelligent design -- in the genome.

Be glad you have ATIII in your bloodstream. It's an anticoagulant, helping prevent thrombosis and pulmonary embolism. It plays a very important role in regulating normal blood coagulation. As a serpin (serine protease inhibitor), its job is to prevent runaway clotting by deactivating a certain protease called thrombin. Behe actually talks about it in his book (p. 85) in the chapter about the blood clotting cascade:

Once clotting has begun, what stops it from continuing until all the blood in the animal as solidified? Clotting is confined to the site of injury in several ways. (Please refer to Figure 4-3.) First, a plasma protein called antithrombin binds to the active (but not the inactive) forms of most clotting proteins and inactivates them. Antithrombin is itself relatively inactive, however, unless it binds to a substance called heparin. Heparin occurs inside cells and undamaged blood vessels.
From there, the complexity of the blood clotting system rises dramatically. Antithrombin (ATIII being the principal form) is thus a key player in this example of what Behe demonstrated to be an irreducibly complex (IC) biological system. In 1996, ATIII's structure was little known. Now, seven molecular biologists are telling us it works like a mousetrap!

But can you be sure ATIII is itself irreducibly complex? First, note that the seven authors of the PNAS paper, all from the University of Massachusetts, never explain how this protein might have evolved. Quite the contrary; their only mention of "evolution" deals with how the protein folds, not with Darwinian evolution. There's no mention of selection, phylogeny, or ancestors. Instead, they seem fascinated by the precise way this machine must be assembled and "cocked" for action. Watch for "mousetrap" again:

Irreversible switching from one conformation to another allows proteins to perform mechanical work without external energy sources such as ATP. Large conformational movements, up to ∼100 Å, can be triggered by proteolysis or changes in environmental conditions, such as pH, initiating processes including membrane fusion for viral infection, protease activation, or inhibition. To facilitate these processes, proteins must fold to kinetically trapped metastable states with relatively high free energy. How proteins fold to these states and avoid more thermodynamically stable conformations is poorly understood. The serpin family of serine protease inhibitors exemplifies this type of metastable protein, and its mechanism of folding presents a conundrum. The native, active serpin fold positions the target protease-binding site on a loosely structured, accessible stretch of sequence termed the reactive center loop (RCL). Once the protease forms a covalent acyl intermediate in the scissile bond in the RCL and cleaves the bond, the serpin undergoes a major conformational change like the springing of a mousetrap, and the protease is carried ∼70 Å to the opposite side of the serpin, thereby inactivating the protease by mechanical deformation (Fig. S1). Strikingly, the conformational landscape of serpins has an alternate fold that is more stable than the functionally required "cocked mousetrap" fold. In this alternative fold, called the latent state, the intact RCL is inserted as an additional strand into the central β-sheet, resulting in a more stable but inactive state.
Are we having fun yet? Here is a molecular machine that must be cocked like a mousetrap, storing energy for its function. In a very real sense, the "mice" that ATIII needs to catch are proteases. Just as a sprung mousetrap is in a more stable state but can't catch mice, ATIII has a more stable thermodynamic state but can't catch proteases. To latch onto and deactivate proteases, ATIII must first be cocked by a precisely operated folding sequence and association with heparin. Only then, when it finds its prey, it "undergoes a major conformational change like the springing of a mousetrap" to deactivate it.

And thus you are kept healthy, neither bleeding to death nor clotting to death. The irreducible complexity of ATIII is also demonstrated by showing what happens when it fails. They found that out by looking at a variety of mutant forms. Keep in mind that in an IC system each part is necessary for function:

Encoding this gymnastic ability in the folding landscape of serpins comes at a risk: Many mutations in serpins cause misfolding and are associated with diseases called serpinopathies.
The serpin antithrombin III (ATIII) plays an essential role in blood clotting by regulating the activity of thrombin and other serine proteases in the coagulation cascade. Numerous misfolding mutations of ATIII are linked to thrombosis. The cellular folding process of ATIII, including its traversal of the secretory pathway, facilitates its folding to the functional metastable high free energy state. The differing outcomes of unassisted refolding of purified ATIII and its cellular folding underline the profound difference between protein folding reactions in isolation and in cells and invite further exploration of the key players and steps that make cellular folding so successful. The fact that ATIII and other serpins must adopt metastable states to function and that their misfolding is implicated in several pathologies further raises the importance of understanding their cellular folding pathway.

The details of the folding pathway need not concern us here, except to note that they are precise and ordered. The easiest thing for this protein to do after it emerges from the ribosome would be to fold into a stable clump that does nothing. That's what happens in test tubes. The reason functional ATIII folds "rapidly and efficiently" in cells, the scientists found, is because it proceeds in a sequence of steps, aided by chaperones. They suspected a conspiracy at work:

We hypothesized that the ER carbohydrate-binding chaperones calnexin and calreticulin may be coconspirators in high-fidelity cellular folding of ATIII. We tested this hypothesis by treatment of ATIII producing cells with the glucosidase inhibitor castanospermine (CST), which prevents the formation of monoglucosylated glycoproteins and thereby inhibits lectin chaperone binding. In the presence of CST, the level of ATIII secreted was reduced by a factor of three (Fig. 3A, lanes 28-36). The activity of the secreted triglucosylated protein was also modestly lower than untreated ATIII (Fig. 3B). Together, these results demonstrate the importance of glucosidase trimming and subsequent lectin chaperone binding for the efficient maturation of functional ATIII.
That gives a modest sense of the overarching lesson here: multiple factors are working together to make ATIII work. This machine, in turn, requires genetic instructions that exhibit specified complexity, or else function is lost. And ATIII is one of multiple factors working together to make blood clotting functional. As biologist Jonathan Wells remarked in Unlocking the Mystery of Life, "What we have here is irreducible complexity all the way down."

Yet more pre Darwinian design v. Darwin

Whether in Bacteria or Humans, Quality Control Systems Operate Everywhere in the Cell.
Evolution News & Views 

earch for the phrase "quality control" in our pages and you will find a lot of entries. Both words, "quality" and "control," fit a model of intelligent design beautifully.

By contrast, why would an unguided Darwinian process care about "quality"? Why would evolution care about "control"? That's especially the case where the two occur in combination. The phrase presupposes a mindful goal of controlling quality. It's always satisfying, therefore, to find these loaded terms in scientific literature, where you notice that invocations of the phrase are inversely proportional to mentions of "evolution." Fancy that.

Let's look at some papers that specifically use the phrase "quality control."

1. "Direct Communication between Cell's Surveillance and Protein Synthesizing Machinery Eliminates Genetic Errors" (Case Western Reserve University). The news item combines ID-friendly concepts of surveillance, communication, synthesizing machinery, and error correction. Here's the phrase we're looking for: "New research out of Case Western Reserve University School of Medicine describes a mechanism by which an essential quality control system in cells identifies and destroys faulty genetic material."

In their work, they ask: how can a cell distinguish between normal messenger RNA and defective mRNA? They describe "evidence for direct communication between the cell's protein synthesis machinery -- the ribosome -- and the protein complex that recognizes and destroys defective genetic intermediates called messenger RNAs (mRNAs)." Direct communication; that's pretty neat. Read all about it in Nature Communications, an open-access journal, which also uses the phrase "quality control." We must share this nifty analogy from the news announcement:

"Consider a car maker," said Baker. "If a faulty brake pedal sneaks past quality control and gets installed into a new car, the primary result is an improperly functioning car, which, in itself, is bad. However, failure to remove the car from the road could have grave secondary consequences if it leads to the damage of other cars, drivers or roads. Efficient quality control processes are therefore necessary, and ones that identify and remove faulty genetic intermediates from the cell are absolutely critical for avoiding downstream consequences that could negatively impact the function of the entire cell."
2. Researchers from Hungary published this paper in the Proceedings of the National Academy of Sciences (PNAS): "Shuttling along DNA and directed processing of D-loops by RecQ helicase support quality control of homologous recombination." The phrase also appears ten times in the body of the paper. The team studied RecQ helicase, one of several enzymes in bacteria and humans that ensure quality control of DNA repair by homologous recombination. It's amazing to find an enzyme that can distinguish between good and bad recombination events and take action.

A major role suggested for RecQ is the selective inhibition of illegitimate recombination events that could lead to loss of genome integrity. How can RecQ enzymes perform an exceptionally wide range of activities and selectively inhibit potentially harmful recombination events? Here, we propose a model in which the conserved domain architecture of RecQ senses and responds to the geometry of DNA substrates to achieve HR quality control." [Emphasis added.]
In the Abstract, the researchers state that DNA damage is inevitable. Cells must continually repair damage "while avoiding the deleterious consequences of imprecise repair," they say. They proposed a model that implicates the geometry of DNA "through which RecQ helicases achieve recombination precision and efficiency."

3. Another paper in PNAS by two researchers from Howard Hughes Medical Institute finds that "Quality control mechanisms exclude incorrect polymerases from the eukaryotic replication fork." They first describe DNA replication as "a central life process and is performed by numerous proteins that orchestrate their actions" to produce two identical copies of the genome before cell division. Notice that they suspect a rational cause behind a mystery:

While the antiparallel architecture of DNA is elegant in its simplicity, replication of DNA still holds many mysteries. For example, many essential replication proteins still have unknown functions. In eukaryotes the two DNA strands are duplicated by different DNA polymerases. The mechanism by which these different polymerases target to their respective strands is understood. This report examines the mechanisms that eject incorrect polymerases when they associate with the wrong strand.
4. Nature published a paper by researchers at the University of Göttingen: "mRNA quality control is bypassed for immediate export of stress-responsive transcripts." We know from human civilization that sometimes you have to sacrifice one good for a greater good -- like survival. A government may have to suspend standard procedures in wartime, for instance, in order to rush ammunition to the front lines. Something like that goes on in cells, which often enter stressful situations.

Cells grow well only in a narrow range of physiological conditions. Surviving extreme conditions requires the instantaneous expression of chaperones that help to overcome stressful situations. To ensure the preferential synthesis of these heat-shock proteins, cells inhibit transcription, pre-mRNA processing and nuclear export of non-heat-shock transcripts, while stress-specific mRNAs are exclusively exported and translated.
We can relate to the analogy with wartime, but how does a cell know to let the emergency responders through? They found that the rules for adaptors change. Non-stress transcripts lose their adaptors so that they cannot be exported. Simultaneously, stress proteins get relaxed permission to exit the gates and get to work. Notice three uses of the phrase "quality control' in this excerpt:

An important difference between the export modes is that adaptor-protein-bound mRNAs undergo quality control, whereas stress-specific transcripts do not. In fact, regular mRNAs are converted into uncontrolled stress-responsive transcripts if expressed under the control of a heat-shock promoter, suggesting that whether an mRNA undergoes quality control is encrypted therein. Under normal conditions, Mex67 adaptor proteins are recruited for RNA surveillance, with only quality-controlled mRNAs allowed to associate with Mex67 and leave the nucleus. Thus, at the cost of error-free mRNA formation, heat-shock mRNAs are exported and translated without delay, allowing cells to survive extreme situations.
Now let's briefly look at a few more papers that imply quality control without explicitly using the phrase.

5. "Acetylation promotes TyrRS nuclear translocation to prevent oxidative damage" (PNAS). Chinese scientists investigated a post-translational modification to Tyrosine tRNA synthetase. This particular member of the synthetase family has a second job: protecting the nucleus against oxidative stress. An acetyl tag lets it relocate to the nucleus, something like a badge that can let a volunteer firefighter get past the traffic cops and through the crowds. "Herein, we report that TyrRS becomes highly acetylated in response to oxidative stress, which promotes nuclear translocation." Here's another bragging right for the twenty-member enzyme family: "many aminoacyl-tRNA synthetases, including TyrRS, have been shown to take on multiple roles."

6. "First-passage time approach to controlling noise in the timing of intracellular events" (PNAS). Timing is another key concept in quality control. In this paper from the University of Delaware, three researchers ask how the cell can keep order in a noisy environment. "Understanding how randomness in the timing of intracellular events is buffered has important consequences for diverse cellular processes, where precision is required for proper functioning." The insights they gain from experiment involve critical levels, feedback regulation, and event triggers. "Formulas shed counterintuitive insights into regulatory mechanisms essential for scheduling an event at a precise time with minimal fluctuations." That's quality control.

7. "Study characterizes key molecular tool in DNA repair enzymes" (Science Daily). From the University of North Carolina at Charlotte come revelations about a component of DNA repair enzymes dubbed Zf-GRF, "which is highly conserved in several enzymes and across species, [and] has been shown to be a key molecular tools [sic] that binds and orients repair enzymes to DNA." Repair, naturally, is a key concept in quality control design. The paper, "APE2 Zf-GRF facilitates 3′-5′ resection of DNA damage following oxidative stress," is published by PNAS.

8. "Histone degradation accompanies the DNA repair response" (Friedrich Miescher Institute for Biomedical Research). Human rapid-response teams need assistants. How well would paramedics operate, for example, without dispatchers and vehicle technicians? The news item for a paper in Nature Structural & Molecular Biology describes quality control of this sort without using the phrase:

DNA repair is paramount for the functioning of every cell and organism. Without it, proteins no longer work properly and genes are misregulated, all of which can lead to disease. It comes therefore as no surprise that the cell devotes enormous resources to detect and repair DNA damage and ensure DNA integrity.

Pretty clear, isn't it? Quality control operates at every level and every location in the cell. By logical implication, so does intelligent design.

Zebrafish v. Darwin

These Fish Have Nose Turbines
Evolution News & Views

We see turbines in wind farms, in generators, and in jet engines. Run a Google search on "turbine" and look at the images. You can't find any that look like random accidents. Instead, almost as a rule, they appear downright elegant, highly sophisticated, and complex. Well, here's a "turbine" inside the nose of a tiny fish. It is no exception.

In Current Biology, a dozen researchers from Europe and Japan tell an amazing story about what they found in four-day-old zebrafish larvae. They actually use the word turbine:

Our data showed for the first time how the motile cilia decorating the nose pit act as a very powerful water turbine and generate strong and robust flow fields that allow fish to quickly exchange the content of the nose. Importantly, this mechanism increases the sensitivity and temporal resolution of odor computations both in stagnant and running aquatic environments and does not require muscle contraction. [Emphasis added.]
Earlier in the paper, they refer to "these microscopic jet turbines" that help fish smell better. (Especially after a few days in the fridge. Ha ha. Thanks, folks, we'll be here all week.)

The paragraph quoted above refers to "motile cilia" which, incidentally, "Revolutionary" biochemist Michael Behe used as illustrations of irreducibly complex molecular machines in Darwin's Black Box twenty years ago (pp. 59ff) and in more detail in The Edge of Evolution (2007, Chapter 5). There are also non-motile cilia -- just as complex -- that work as sensory antennae on most vertebrate cells. The motile cilia, by contrast, are fun to watch, because they move like whips. The hair-like projections on ciliated cells slide along the membrane for the wind-up, then extend fully for a power stroke. This goes on in your windpipe right now, sweeping dust out and keeping your airways clean. The cilia beat in a coordinated fashion, creating waves that collectively move particles along a train of flow, more powerful than a single cilium could accomplish alone. No one knows how they do that (e.g., Live Science).

If you recall the animation of salmon olfaction in Illustra's film Living Waters (watch it again here), you remember seeing non-motile cilia rising out of the olfactory epithelium, the tissue inside the nose. Those are the cilia on olfactory receptor neurons (ORNs) that latch onto odorant molecules and send the information down molecular "wires" (neurons) to the olfactory bulb (OB). In the olfactory bulb, the collected information is sorted into combinatorial codes that classify tens of thousands of different odorants before sending the processed information to the brain.

What the film doesn't show is what this paper now reveals. Surrounding the epithelium are cells with motile cilia. Beating in synchrony, they create a flow of water, just like a turbine. This dynamic flow -- requiring no muscles -- accomplishes several functions. First, it draws water into the nose, even in stagnant water or when the fish is idle. Second, it creates a flow pattern that directs odorant molecules over the sensory neurons and then out to the sides. This increases the sensitivity of the sense of smell dramatically. Third, the flow pattern helps the fish detect changes in odor patterns much more rapidly than it could otherwise (i.e., it increases the temporal resolution of the fish's sense of smell). The paper's title sums this up: "Motile-Cilia-Mediated Flow Improves Sensitivity and Temporal Resolution of Olfactory Computations."

Computations? Yes, that's what goes on in the fish's brain as it processes the combinatorial codes sent from the olfactory bulb. Visualize that salmon swimming upriver, trying to follow a faint trail of odor molecules on its way to its natal stream. Obviously, the eager fish can do a better job of computation if the information comes in faster. The ciliary turbine helps the fish turn up its response time, whether it's hanging out idle or swimming rapidly to get home.

Our measurements showed that fluctuating odor stimuli with decreasing inter-stimulus intervals are sampled significantly faster and with higher temporal resolution at the nose pits of controls [wild-type fish].... In line with these findings, we observed that odor fluctuations are encoded significantly better at the level of the olfactory bulbs at all inter-stimulus intervals by control animals.... In fact, increasing the difficulty of the task by challenging the animals with faster odor fluctuations led to more significant differences in temporal encoding of odors by the OB neurons of control animals....
Young zebrafish provide an ideal way to observe this, because when the larvae are about four days old, their noses are shaped like little cups. It's one of the few places in nature where scientists can watch motile cilia at work in a live animal. In a series of clever experiments, the researchers set out to test the hypothesis that fish smell better with cilia turbines. They used wild-type as controls, and mutants without motile cilia for testing.

Do the motile cilia beat with a measurable frequency? Check. Yes, about 25 Hz.

Do the cilia cooperatively draw water into the nose? Check.

Does the flow pattern draw particles over the olfactory neurons? Check.

What is the average dwell time of an odorant on the epithelium? About 0.4 seconds.

Where does the flow go after flowing over the epithelium? Out to the sides.

Is the flow pattern caused by the motile cilia? Check. Mutants with paralyzed cilia lack the flow pattern.

Is a similar turbine system found in young salmon? Check; it's not unique to zebrafish.

Does the flow pattern increase activity in the olfactory bulb? Check. Passive diffusion of odors had a much lower response in the mutant fish.

Is the response better when an artificial flow is introduced into the nose? No; mutant fish can respond just as well to water flowing into the nose, but they suffer in stagnant water or when not swimming. Moreover, the dwell time of each odorant is increased, reducing temporal resolution.

Do rapidly fluctuating odor plumes introduced into the water show up in the OB? Check. The flow pattern appears to increase the temporal sensitivity to rapidly changing odor plumes. When pulses of odors are introduced every 2, 4, or 8 seconds, the response changes accordingly in wild-type. Mutants, however, suffer a delay in odor arrival and have longer odorant dwell times, decreasing temporal resolution in dynamic environments.

Here's how they summarize their main findings:

Thanks to the optical accessibility of zebrafish nose pit, we could fully characterize how motile cilia beat to generate a robust flow in an intact organism. First, the asymmetric beating pattern that we show for the motile cilia of the nose is conserved across many MCCs [multi-ciliated cells] located along the brain ventricles, spinal cord, and respiratory tract. Second, the average CBF [cilia beat frequency] of zebrafish and salmon olfactory MCCs is rather uniform across individuals and lies between 19 and 30 Hz.... Third, we showed that flow characteristics resulting from the specific location and asymmetric beating of motile cilia are tailored to the organ's need. In the brain ventricles, beating cilia can concentrate molecules locally or prevent entry to another ventricular area by generating boundaries. Our findings suggest here that the robust and directional flow, generated by motile cilia in the nose pit, guarantees an efficient exposure of ORNs to odors but for a restricted time. Even though it is now clear that fluid dynamics are regulated by the power and directionality of ciliary beating, the cellular and molecular mechanisms underlying the establishment of asymmetric ciliary beating remain to be fully understood.
So after twenty years, Behe will still have more to write about these amazing molecular machines. The researchers point out that similar principles may operate in mammals and humans. You, too, could have turbines in your nose... wind turbines!

The authors introduce evolutionary speculations at several points. For one, they make a big deal of the fact that motile cilia show up all over the place: in the brain, in the airways, and in fish noses.

It is an intriguing correlation that the motile cilia in the nose of most vertebrates and in the airways of mammals generate ciliary beating with similar principles, highlighting a possible evolutionary relationship between these structures.
Yet they have to admit that cilia are "conserved across most vertebrate species from fish to rodents." That's not evolution; that's stasis. For another piece of evidence, they point out differences between zebrafish and more "primitive" creatures:

As an alternative solution, a few aquatic vertebrates evolved accessory sacs in their olfactory organs that can be expended and compressed. Lobsters were shown to move their antennules to draw water into the olfactory epithelium.
Later in the paper:

Interestingly, in hagfish and lampreys, which are considered evolutionarily primitive fish species, the respiratory flow initiated by the velum contraction passes through the olfactory chamber toward the gills and thus draw odors. Thus, from an evolutionary perspective, it appears that cilia-driven flow in the nose pit is rather novel and may underlie a powerful and energy-efficient mechanism to draw odors into the nose. Altogether, we propose that this mechanism might have evolved to facilitate better sampling of dynamically changing odor plumes and thereby enhance the temporal resolution of olfactory computations.
There are at least two difficulties here. One is that different mechanisms that achieve a common function make the problem worse for Darwinian evolution. It multiplies the number of chance mutations that had to be selected. Another is the statement that a "mechanism might have evolved to" do something useful. Darwinian evolution has no foresight. It has no goal. It cannot order and direct mutations to conspire to work together to create a novel "powerful and energy-efficient mechanism," particularly one as irreducibly complex as a cilium. The authors don't even begin to address the complexity of a single cilium.

The irreducible complexity doesn't stop there. The cilia in a tissue have to work in concert. They have to line up in certain locations in the nose to create the flow pattern. And the brain has to be tuned to respond rapidly enough to the increased rate and lower dwell times of each odorant. The authors are fully aware, furthermore, that damaged cilia cause serious problems, just as they did with the cilia-defective mutant fish.

Cilia are microscopic hair-like structures extending from the surface of almost all cells of the vertebrate body. Motile cilia actively move and drive directional flow patterns across tissues, whereas primary cilia are enriched in receptors and play crucial sensory roles. It is therefore not surprising that mutations affecting the structure, function, or presence of cilia result in multiple human pathologies, collectively known as ciliopathies.

These evolutionary speculations aside (which, by the way, stand in contrast to their exemplary lab work), we can step back and appreciate this new discovery that adds another level of complexity and elegance to what we already knew about fish olfaction. Are turbines intelligently designed? Try to think of one that isn't.

A clash of Titans. XLV

Israel is committing suicide via settlements?:Pros and cons.

Time for the Palestinian flag at the U.N?:Pros and cons.

On the fall of man:Non-theist edition.

Darwin, Marx, and Freud: The Genealogy of "Posthumanism"
David Klinghoffer

Wesley Smith  points out  the simultaneously vapid and dangerous  musings of Rice University scholar Cary Wolfe on "posthumanism." That is the idea that we can and should progress beyond the ancient understanding that something fundamental separates human beings from other creatures and from the rest of nature.

Where does posthumanism come from? Wolfe is admirably frank about its "genealogy":

There is, in fact, a genealogy of posthumanist thought that stretches back well before the 21st or even 20th century. You find hints of it in anything that fundamentally decenters the human in relation to the world in which we find ourselves, whether we're talking about other forms of life, the environment, technology or something else. Perhaps more importantly, you find it in the realization that when you don't allow the concept of the "human" to do your heavy philosophical lifting, you are forced to come up with much more robust and complex accounts of whatever it is you're talking about. And that includes, first and foremost, a more considered concept of the "human" itself.

...

Darwinian thought was a huge step in this direction. So was Marx's historical materialism or the Freud of "Civilization and Its Discontents." [Emphasis added.]


Darwin, Marx, and Freud -- the trio who did so much to give us modern culture with its deformities. Exactly how posthumanism cashes out in contemporary cultural terms is the subject of a detailed studied by John G. West, ""Darwin's Corrosive Idea: The Impact of Evolution on Attitudes about Faith, Ethics, and Human Uniqueness." Download it now.

Yet another layer of design?

Cornell Researchers Find Another Epigenetic Code that Affects Messenger-RNA Productivity
Evolution News & Views

"Research reveals codes that control protein expression." That's the attention-getting headline of an article at the  Cornell Chronicle. Researchers from Weill Cornell Medicine led by Dr. Samie Jaffrey found another signaling system that predetermines how much protein a transcribed gene should generate.

The findings may settle a fundamental question in molecular biology -- how the amount of protein generated from a messenger RNA (mRNA) is determined -- and could help scientists develop new therapies for diseases such as cancer where abnormal amounts of protein accumulate.
"This is one of the biggest questions in molecular biology," said senior study author Dr. Samie Jaffrey, the Greenberg-Starr Professor and a professor of pharmacology at Weill Cornell Medicine. [Emphasis added.]

Here's how it works. At the 5' end of a messenger RNA transcript, there's a "cap" region. This cap region was previously thought just to provide a docking structure when the mRNA enters the ribosome, but it turns out that it can also hold information. If the cap has an adenine base (the A in the genetic code), the adenine with its attached sugar ribose (adenosine) can hold up to two methyl groups, which are tags made up of CH3. If the adenosine has one methyl group, it is called m6a. If it has two, it's called m6am. This provides a signaling system for the cell. Think "one if by land, two if by sea."

Jaffrey and team, publishing in Nature, proved experimentally that m6am messenger RNAs are more stable. This means they are more likely to survive longer in the cell and generate more copies of their corresponding protein. Normally, mRNAs are short-lived, degraded by the cell after they produce a protein. That's what happens to the singly methylated m6a forms. If it has the double methyl tag (m6am) it will last much longer and produce more protein. Lindsey explains why stability is related to protein abundance:

They found that mRNAs with m6Am "were highly expressed, meaning that these mRNAs are highly abundant in the cell," Jaffrey said. "They were translated at higher levels and persisted in the cell for a very long time."
Many of these mRNAs contained instructions for making proteins that support cellular metabolism, survival and growth, and these proteins are typically essential for cellular proliferation.

Another player is involved in this coding scheme. It's called FTO ("fat mass and obesity associated protein"). This enzyme can remove methyl groups from the cap adenosines, but it mostly goes after the doubly methylated m6am forms. Because of this, FTO regulates the stability of mRNAs. The Cornell team found that FTO was 100 times more likely to remove a methyl tag from m6am than from m6a.

And then there's another player: DCP2. This enzyme "decaps" mRNAs, facilitating their degradation. Once decapped, mRNAs are degraded by micro-RNAs. The m6am RNAs, however, are more resistant to decapping by DCP2. This new epigenetic code helps explain why some mRNAs are more robust against degradation than others.

Why is this important? Without this signaling system, bad things can happen!

Since m6Am promotes cell growth and proliferation, abnormalities in FTO and m6Am levels can potentially contribute to cancer by encouraging uncontrolled cell division and by making it difficult for malignant cells to die.
"We've known for years that FTO is a critical regulator of cell function," Mauer said. "Misregulated FTO is associated with severe developmental defects and diseases such as cancer."

In their own words, the researchers consider this a coding system. "An internal code in cellular molecules called messenger RNA predetermines how much protein they will produce," Lindsey says. In the paper, the authors explicitly use the words code and information. In the Introduction, they say this:

An emerging concept in gene expression regulation is that a diverse set of modified nucleotides is found internally within mRNA, and these modifications constitute an epitranscriptomic code.
And they repeat the concept in the concluding Discussion:

Here we identify m6Am as a dynamic and reversible epitranscriptomic mark. In contrast to the concept that epitranscriptomic modifications are found internally in mRNA, we find that the 5′ cap harbours epitranscriptomic information that determines the fate of mRNA. The presence of m6Am in the extended cap confers increased mRNA stability, while Am is associated with baseline stability. m6Am has long been known to be a pervasive modification in a large fraction of mRNA caps in the transcriptome, making it the second most prevalent modified nucleotide in cellular mRNA. Dynamic control of m6Am can therefore influence a large portion of the transcriptome.
Interestingly, the code is also location-dependent:

The concept of reversible base modifications is appealing since it raises the possibility that the fate of an mRNA can be determined by switching a modification on and off. Our data show that FTO is an m6Am 'eraser' and forms Am in cells. FTO resides in the nucleus, where it probably demethylates nuclear RNA and newly synthesized mRNAs. Demethylation of cytoplasmic m6Am mRNAs may be induced by stimuli that induce cytosolic translocation of FTO.....
.... Thus, the location of the modified nucleotide and the specific combination of methyl groups on adenosine residues encode distinct functional consequences on the mRNA.

The essence of a "code" is that it bears information. This code resembles an "if-then" algorithm in software. Speaking mechanistically, there's nothing about a methyl group that should indicate, "keep this attached molecule stable against degradation." Instead, the coding system works because all the players recognize the convention.

The methyltransferase enzyme has to "know" which mRNA needs a second methyl group to confer stability, because it has an essential role. The FTO enzyme "knows" to concentrate on demethylating one tag from the m6am forms, and to stay inside the nucleus unless stimulated to go after m6am RNAs in the cytoplasm. And DCP2 has to know to avoid uncapping the doubly-methylated m6am transcripts. Because the players know the signal, the cell produces the appropriate quantity of proteins corresponding to their importance.

What we see here is another Signature in the Cell. Intelligent design advocates are not surprised to find codes and switches in irreducibly complex systems. In fact, we expect that this finding will stimulate the discovery of additional codes, such as those that decide which mRNA transcripts should be treated as more important than others.


Darwinian evolution, by contrast, has a big challenge in explaining how multiple players mutated together by chance to hit upon a language convention. What do unguided, blind processes know about codes? What do they understand about information? In short, nothing.

Salamanders v. Darwin.

Salamander Offers Two Evolutionary Quandaries: Non-Homologous Development and an ORFan
Cornelius Hunter

Salamanders have their own way of doing things. For most animals, if an important body part, such as a limb, is lost, it is gone for good. But for salamanders, they just grow a new one. Also, salamanders use different embryonic development patterns. For example, their digits (fingers and toes for us humans) form in the wrong order -- going, essentially, in the wrong direction.

You can see this from a figure in a  paper  by Neil Shubin's group. In the figure, the numbers across the top show the order in which the digits appear. Salamanders go against the common pattern. This "reverse polarity" in what otherwise is a highly conserved development pattern in the tetrapods is a quandary for evolution.

Early evolutionists who first seriously reckoned with this "striking deviance from an otherwise conserved pattern in tetrapods," as the Shubin paper puts it, as well as other distinctive features of salamander limb development, concluded that the salamanders probably arose independently of the other tetrapods. In other words, these development inconsistencies were so profound they required an independent origin -- there were two different origins of tetrapods.

The problem, however, is the set of similarities between the salamanders and their cousin tetrapods is so massive that any such independent origins would be absurd from an evolutionary perspective.

So evolutionists were left needing an explanation for the profound divergence. Perhaps salamanders got their start with a loss of digits. If the first salamanders had only two digits, and then re-evolved the other digits (catching up to their ancestral forms), the development order could have been rearranged.

Unfortunately such a hypothetical evolutionary history, where the salamanders begin by losing digits, does not fit the data (both molecular and fossil) very well, even within the context of evolutionary theory.

Perhaps the salamander digit development deviance arose as a larval adaptation. Or perhaps the salamander development pattern is not a "deviance" at all, but rather is the nominal, ancient pattern, but is retained only in salamanders among living tetrapods.

But these hypotheses have problems as well. In fact the salamander character data are full of contradictions:

The evolution and phylogeny of crown group salamanders is plagued by homoplasy. In fact, a large a number of highly derived anatomical characters, including body elongation, tail autonomy, and life history pathways, have been demonstrated or are debated to have evolved multiple times.
(Note that these anatomical characters have not "been demonstrated" to have evolved multiple times. That is a misrepresentation of the science. They only have "been demonstrated" to have evolved multiple times if one assumes evolution at the outset.)

Yet another problem plaguing these evolutionary hypotheses is the finding of genes unique to the salamander that are crucial for its limb regeneration ability and unique embryonic development patterns. You can read more about these here and here and this brings us to the second half of our two-fer.

Whether they are called unique genes, novel genes, orphans, ORFans, taxonomically-restricted genes (TRGs), lineage-specific genes (LSGs), or whatever, they are a problem for evolution. First, they counter the above hypotheses attempting to explain the salamander's unique development. As one paper explains:

[T]he notion of an ancient limb regeneration programme has been challenged by reports of salamander lineage-specific genes (LSGs) upregulated during regeneration. One salamander LSG in particular, the Prod1 gene, was shown to be required for proximodistal patterning during limb regeneration and for ulna, radius and digit formation during forelimb development. The existence of urodele LSGs expressed and involved in regeneration has lent support to the hypothesis that limb regeneration is a derived urodele feature.
In other words, the salamander gets it done using genes unique to its lineage, and that contradicts the hypothesis that the salamander's unique capabilities were there all along.

It also contradicts the evolutionist's longstanding, but rapidly fading, hope that ORFans would go away. As I have  explained, evolutionists hoped that such lineage-specific genes would be found in other species as more genomes were decoded. But instead the number of ORFans just continued to grow.

Evolutionists next predicted that similar ORFan sequences would be found in the so-called non-coding DNA. Although that is sometimes the case, it is not generally, and the Prod1 gene is another example of this.

Evolutionists next predicted that ORFan sequences were probably not part of a mature protein-coding gene and did not form functional proteins. That also is wrong, and Prod1 is yet another example of an ORFan that is indeed a real protein.

The findings of unique (non-homologous) development patterns, and lineage-specific genes make no sense on evolution. And attempts to explain these findings according to evolution with clever, detailed hypotheses just cause more problems.


If you try to build a house on a faulty foundation, it will just get worse. Evolution is a flawed theory, and the more we learn about biology, the more evident that becomes.

Darwinian devolution.

Titan v. Future Titan.

Man's best friend paying the price for our aesthetics.

Equal rights for unborn women?Pros and Cons.

Whale fossils not sticking to Darwinism's script.

Fake Science: Whales as the "Sweetest Series of Transitional Fossils" an Evolutionist Could Ask For
David Klinghoffer 

Over the New Year's Day holiday my family and I took in the new IMAX feature Voyage of Time  from Terrence Malick. I had been  looking forward to that and was not disappointed. It's spectacular visually, and a compelling, unsettling presentation of the director's vision of life, its history and future.

My wife thought the narration by Brad Pitt was a bit "cheesy." That was not because of any shortcoming of Mr. Pitt's but because Malick's script consistently elides the question of how animals transition from one form to another. As he tells the story, major new forms of life are continually "arising" as if out of nowhere. "Arose" seemed to be pretty much Mr. Malick's favorite word in the whole film, pronounced with a stately majesty by Brad Pitt.

I don't fault Malick for this at all, though. In fact, I wonder if the folks at Seattle's Pacific Science Center, where we saw the film, noticed that it makes not one reference to Darwinian explanations. Admitting that things like whales (and much else) appear in the fossil record without plausible ancestors is the beginning of wisdom when it comes to evolution.


Whales nevertheless remain a notable evolutionary icon. They're not Malick's focus, of course, but no account of evolution is complete without confronting the problem they present. And what do you know -- in a series of interviews for ID the Future, our biologist colleagues Jonathan Wells and Ray Bohlin do just that, launching into a detailed deconstruction. Part 1  is up now.
Back in the day, paleontologist Stephen Jay Gould found in whales "the sweetest series of transitional fossils an evolutionist could ever hope to find." No doubt it honestly looked that way to him, but no longer.

Not that that keeps popular and science media from invoking whales on behalf of Darwinism. In truth, the "picture-perfect intermediacy," which Gould commended as a weapon to be deployed against "creationists," looks increasingly like a patchwork. The situation was made worse by the recent documenting of a 49-million-year-old Antarctic whale jawbone fossil that narrowed the window available for the evolution from a fully terrestrial ancestor to an unbearably rushed 1 million years.


Whales as a poster child for Darwin are looking like another case of evolutionary fake science, right up there with the   myth of a 99 percent equation between chimp and human DNA.

On the difference between technology and magic.

Intelligence Is Not Magic. It's a Cause We Know.
Evolution News & Views

Thought experiment: You are a science writer for the Land of Ozma (Ozma being a fictional queen of note in the history of SETI). Your assignment is to explain the origin of life without reference to intelligent design for your munchkin readers, who are all looking to you for enlightenment. The munchkins have a natural inclination to believe in a designer behind the life they see all around them, but they have been taught in school that life emerges naturally. Your job is to reassure them that it does.

One big problem stares you in the face before you write. It's the hard, cold mathematics of probability. As Illustra Media shows in their recent film Origin, getting one functional protein to self-assemble without design is so outrageously, mind-blowingly, inconceivably improbable that it will never happen in uncountable quintillions of universes under the most ideal conditions imaginable -- and that's an understatement! Even if it did happen, it would be one lifeless protein. The same problem exists for DNA, RNA, and the other information-rich molecules of life. Tim Standish is overly kind when he remarks in the film that getting all the components for life in one little membrane-bound compartment at the same place and time is "the next best thing to impossible."

Facing this small difficulty, what do you do? The smart thing would be to quit, saying, "Take this job and shove it" as you storm out the door. Assuming this is your chosen livelihood, however, you can still get paid by using some rhetorical tricks (remember, the job is not to prove it happened, but just to reassure the munchkins it might have happened). If you're looking for a master magician to show you the ropes, you can hardly do better than to follow the example of Michael Gross, a science writer in Oxford, England, who pulls multiple rabbits out of hats in a feature for Current Biology, "How life can arise from chemistry." He tells readers that rabbits naturally emerge from hats without magic. Here are some principles extracted from his article.

Ridicule anyone else's position. Munchkins may become unsettled if they see any other teachers around, so all other contenders must be disqualified. Gross dispenses with them right in his first paragraph, using the straw man tactic. "Life, in many people's view, is special and different from all non-living matter to an extent that ancient cultures tended to credit its existence and astounding diversity to an almighty creator" (emphasis added). No modern munchkin wants to identify with "ancient cultures." In one masterful stroke, Gross equates belief in a creator with being behind the times. He rubs it in with a medieval-looking painting of God calling life into being.

Roll call some heroes. Name-dropping helps you appear to be in good company, even if the names did nothing to help solve the origin of life. Gross conjures up some familiar faces: "Since then [ancient times, that is], Darwin and his successors have rationalised the diversity, Wöhler [who synthesized urea] has shown that the molecules of life are chemicals like everything else, and science has abandoned the ancient concept of a vis vitalis or life force that was supposed to set living matter apart." Notice the use of ancient again.

Side with science, not philosophy. Don't let on that science and philosophy are inseparable. The munchkins need to feel that you intend to tell them about "science" as opposed to "philosophy," which Gross lumps in with religion -- a matter of faith, not fact. Here's how Gross gets the ID folk out of the way, lumping them with the other throwbacks from ancient times:

And yet, to this day, some philosophically inclined authors like to emphasize the 'sense of purpose' of living beings, a resurgent vis vitalis now known as teleonomy, and argue that Darwin does not reveal how organisms 'purposefully' using energy to counter the unifying effects of entropy may have arisen from purely chemical systems simply obeying the laws of thermodynamics.
Cultivate the imagination. We see Gross tickling the imagination in the previous quote, suggesting life "may have arisen" on its own. He continues this practice throughout the article, using may have ten times and could another ten times, along with a smattering of superwords that leap tall impossibilities in a single bound, using the power of suggestion.

Hide your materialism. Materialism? What materialism? I'm not doing philosophy, Gross thinks, when he says that life "may have arisen from purely chemical systems simply obeying the laws of thermodynamics." That's just simple chemistry, not philosophy.

Promise progress. A good rhetorician helps the audience feel they are getting warmer solving a puzzle together. Long forgotten are those laughable probabilistic odds. We're better than those who need that medieval God, he assures the munchkins. We stand with progress! We stand with science! We're getting closer to our goal of understanding! "Rapid progress in investigations into the origin of life is adding to our understanding of how the emergence of evolving systems from prebiotic chemistry may have happened -- without the need for magic." Emergence. Interesting word. Sounds kind of magical.

Hide your party politics. Notice his use of "believed" in the following sentence: "Recently, however, progress in understanding and recreating elements of the RNA world, believed to have been an evolutionary phase preceding and enabling the emergence of DNA and proteins, has advanced to a point where an understanding of how life might arise -- on our planet or on one of the many others that are now being discovered -- comes within our grasp." Believed? Believed by whom? By materialists, of course. Use of a passive voice verb keeps Gross from having to identify the believers. (This one sentence is densely packed with several of the rhetorical tricks above.)

Use jargon sparingly. Toss in a few unfamiliar words here and there to create an air of sophistication, even if they have nothing to do with the main problem of getting life by chance. Create a "eutectic mix" with ammonium formate; add some formidopyrimidines to the mix, etc. But don't overdo this tactic; your goal is to make everything look simple. Assure them that the "'nightmare' of highly heterogeneous mixtures of chemicals" that pioneers dealt with "may be more manageable than thought." Thought? Thought by whom? By materialists, of course. Progress is in the air! "the RNA world has emerged as a plausible and practical model enabling scientists to study many aspects of the early evolution of life and the functioning of simple life forms," Gross assures readers, furthering an "optimistic view" of the origin of life.

Use your enemy's gun. Notice this trick; he discounted the idea of a "life force," but then turns around and imagines something equivalent: "the initial spark" that ignited life. See this word in the next quote, too.

Remain confident. Gross knows that bravado can backfire, so he backpedals just a bit toward the end. It's OK to admit a little ignorance, as long as you keep the myth of progress going, and pound the pulpit as necessary. Don't ever say "I don't know." Say "We don't know." That brings the munchkins into the collective ignorance. Misery loves company, after all.

We may never know how the spark was lit [Lit? Lit by whom?] that led to some kind of molecular self-propagating, evolving system and onwards to the RNA world and more complex cellular life. Indeed, it is hard to imagine a way in which this initial breakthrough could have left a trace that we might detect.
The important part is, however, that it did happen. It may have happened multiple times in different versions, but seeing that the successful ignition meant an onwards progression of exponential proliferation, a single spark followed by four billion years of evolution would be more than sufficient to explain the entirety of today's biosphere. Even though we may never find a trace of that spark, synthetic chemical thinking can provide us with realistic models of how it may have happened on our own planet and on many others.

The important thing is that it did happen! The impossible odds were overcome! It happened somehow! No magic needed!

We could go on with other tricks of the trade in this article, but you get the point. Gross is an absolute master. He completely ignores the elephant in the room, the probability case against materialism described earlier. Not one aspect of the origin-of-life experiments he describes bears on the question of probability. That question obliterates everything else in his toolkit, making his article an exercise in pure rhetoric, convincing readers that the impossible is somehow possible, given enough imagination.

Gross champions the RNA world, neglecting to tell his readers that Harold S. Bernhardt called it "The worst theory of the early evolution of life (except for all the others)." In Origin, Discovery Institute biologist Ann Gauger explains how delicate RNA is, making it useless for origin-of-life models. Additionally, ribose is devilishly hard to synthesize in plausible early earth conditions, where all kinds of undesirable cross-reactions would quickly destroy it. But worst of all is the sequencing problem: without intelligent guidance, its only "information" must come about by chance -- the same impossibility as with proteins. With these problems in mind, look how Michael Gross explains where the RNA came from: "This could have happened directly, or via some simpler form of evolving molecular system yet to be identified." And this is to be sanctified with the name "science"? Gross has cleared the room of magicians, only to play master magician himself.

Had enough? There's more. Listen to his last sentence: "We [we?] can conclude from all of this that the emergence of life in a universe that provides a suitable set of conditions, like ours does, is an entirely natural process and does not require the postulate of a miracle birth." Take that, you Christian readers out there. Actually, your miracle is too tame for Gross. He multiplies unguided miracles ad infinitum, saying they happen everywhere all the time, by chance.


If you like scientific realism, watch Origin, along with our films Revolutionary, Fire-Maker, and The Information Enigma. Intelligence is neither magic nor a miracle. It is the only cause we know that explains the complex specified information that is abundantly evident in this phenomenon we call life.